Objectives: 1. Investigation of the role of inhibitory (hippocampal) and stimulatory (amygdalar) central nervous system (CNS) pathways in ACTH regulation by: a. Assessing the role of such areas with regard to corticosteroid circadian periodicity (CP) and hypothalamic-pituitary-adrenal (HPA) response to stress and steroid feedback. b. Studying the role of alpha and Beta receptors in such ACTH regulation. c. Hippocampal ablation to create an animal experimental model of Cushing's syndrome (CS). d. Reversing the clinical and laboratory features of human CS by increasing CNS levels of serotonin (a postulated amygdalar inhibitory agent) or norepinephrine (NE) to increase postulated central adrenergic inhibition). 2. Study of the effect of alteration of neonatal steroid milieu on the subsequent appearance of adrenal circadian periodicity. Methods: 1a. Production of hippocampal and amygdalar lesions (rat) and observing their effect on CP and HPA response to stress and steroid feedback. b. Administration of alpha and Beta adrenergic blocking agents and observing effect on CP and HPA response to stress, steroid feedback; and pituitary-adrenal response to vasopressin (human). c. Total bilateral hippocampectomy (cats) with pre- and chronic post- operative measurement of parameters of HPA axis known to be abnormal in CS. d. Administration of L-5hydroxytryptophan (to increase CNS serotonin) or L-DOPA (to increase CNS NE) to subjects with active CS, and observing effect on abnormal parameters of HPA axis and growth hormone in such patients. 2. Parenteral administration of corticosteroids early (days 2-5) and late (days 12-14) in the neonatal period and observing the effect on subsequent development of CP and HPA stress responsiveness (rat).